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implicate Asxl1 in the maintenance of podocyte structure via its association with Wtip (show WTIP Proteins) and in the regulation of WT1 (show WT1 Proteins) signaling during early kidney development
ASXL1 truncation mutations confer gain-of-function on the ASXL-BAP1 (show BAP1 Proteins) complex.
Asxl1-/- fetuses have reduced body weight and display cleft palate, anophthalmia as well as ventricular septal defects and a failure in lung maturation.
Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis
C-terminal-truncating Asxl1 mutations inhibited myeloid differentiation and induced myelodysplastic syndrome-like disease
Constitutive loss of Asxl1 results in developmental abnormalities, including anophthalmia, microcephaly, cleft palate, and mandibular malformations. Hematopoietic-specific deletion results in cytopenia and dysplasia with increased hematopoietic stem cells
ASXL1 represses, whereas ASXL2 increases, the expression of adipogenic genes, most of which are PPARgamma (show PPARG Proteins) targets
Asxl1 is needed for normal hematopoiesis.
Asxl1and Asxl2 are expressed as multiple transcripts, at varying levels, in adult tissues and in embryonic stem cells analyzed by Northern blot, and exhibit similar expression patterns suggesting they may be co-regulated
ASXL1 is a novel coactivator of RAR (show RARA Proteins) that cooperates with SRC-1 (show NCOA1 Proteins)
Mutations in ASXL1, U2AF1 (show U2AF1 Proteins), and SF3B1 (show SF3B2 Proteins) are common in Chinese patients with myelodysplastic syndromes.
ASXL1 germline missense substitution is associated with hematological malignancies.
identified significant ASXL1 SNPs in Chinese patients with acquired aplastic anemia (AA); results showed 8.2% had the recurrent conjoined rs62206933, rs117901891 and rs74638057 genotype (WT1 (show WT1 Proteins)), which was closely associated with poor prognosis in patients with nonsevere AA and had a greater risk of transformation to myelodysplastic syndrome
Correction of ASXL1 driver mutation in leukemia cells using CRISPR/Cas (show CSE1L Proteins) increases survival in vivo in mice.
We confirm the negative prognostic impact imparted by ASXL1 mutations and suggest a favorable impact from TET2 mutations in the absence of ASXL1 mutations.
Frameshift mutation in the ASXL1 gene is associated with Bohring-Opitz syndrome.
De novo mutation in ASXL1 gene is associated with Bohring-Opitz syndrome.
Tumor suppressor ASXL1 is essential for the activation of INK4B (show CDKN2B Proteins) expression in response to oncogene (show RAB1A Proteins) activity and anti-proliferative signals
the present results indicate that the truncating ASXL1 mutant is indeed expressed in MDS (show PAFAH1B1 Proteins) cells and may play a role in MDS (show PAFAH1B1 Proteins) pathogenesis not previously considered.
Chronic myelomonocytic leukemia has an inherent tendency to transform to acute myeloid leukemia (show BCL11A Proteins). Gene mutations involving ASXL1 are frequent and identified to have an independent negative prognostic effect on overall survival.
This gene is similar to the Drosophila additional sex combs gene, which encodes a chromatin-binding protein required for normal determination of segment identity in the developing embryo. The protein is a member of the Polycomb group of proteins, which are necessary for the maintenance of stable repression of homeotic and other loci. The protein is thought to disrupt chromatin in localized areas, enhancing transcription of certain genes while repressing the transcription of other genes. The protein encoded by this gene functions as a ligand-dependent co-activator for retinoic acid receptor in cooperation with nuclear receptor coactivator 1. Mutations in this gene are associated with myelodysplastic syndromes and chronic myelomonocytic leukemia. Alternative splicing results in multiple transcript variants.
additional sex combs like 1
, additional sex combs-like protein 1
, putative Polycomb group protein ASXL1